Developing reliable, quantitative conduit models that capture the physical processes governing eruptions is hindered by our inability to observe conduit flow directly. The closest we get to direct evidence is testimony imprinted on individual crystals or bubbles in the conduit and preserved by quenching during the eruption. For example, small crystal aggregates in products of the 1959 eruption of Kīlauea Iki, Hawaii contain overgrown olivines separated by large, hydrodynamically unfavorable angles. The common occurrence of these aggregates calls for a flow mechanism that creates this crystal misorientation. Here, we show that the observed aggregates are the result of exposure to a steady wave field in the conduit through a customized, process-based model at the scale of individual crystals. We use this model to infer quantitative attributes of the flow at the time of aggregate formation; notably, the formation of misoriented aggregates is only reproduced in bidirectional, not unidirectional, conduit flow.In van der Waals heterostructures, electronic bands of two-dimensional (2D) materials, their nontrivial topology, and electron-electron interactions can be markedly changed by a moiré pattern induced by twist angles between different layers. This process is referred to as twistronics, where the tuning of twist angle can be realized through mechanical manipulation of 2D materials. Here, we demonstrate an experimental technique that can achieve in situ dynamical rotation and manipulation of 2D materials in van der Waals heterostructures. https://www.selleckchem.com/products/nocodazole.html Using this technique, we fabricated heterostructures where graphene is perfectly aligned with both top and bottom encapsulating layers of hexagonal boron nitride. Our technique enables twisted 2D material systems in one single stack with dynamically tunable optical, mechanical, and electronic properties.Arterial tortuosity manifests in many conditions, including hypertension, genetic mutations predisposing to thoracic aortopathy, and vascular aging. Despite evidence that tortuosity disrupts efficient blood flow and that it may be an important clinical biomarker, underlying mechanisms remain poorly understood but are widely appreciated to be largely biomechanical. Many previous studies suggested that tortuosity may arise via an elastic structural buckling instability, but the novel experimental-computational approach used here suggests that tortuosity arises from mechanosensitive, cell-mediated responses to local aberrations in the microstructural integrity of the arterial wall. In particular, computations informed by multimodality imaging show that aberrations in elastic fiber integrity, collagen alignment, and collagen turnover can lead to a progressive loss of structural stability that entrenches during the development of tortuosity. Interpreted in this way, microstructural defects or irregularities of the arterial wall initiate the condition and hypertension is a confounding factor.Antiplatelet agents offer a desirable approach to thrombosis prevention through the reduction of platelet reactivity. However, major bleeding events greatly attenuate the clinical outcomes of most antithrombotic agents. Therefore, the development of safer and more effective strategies to prevent vascular occlusion and avoid bleeding is urgently needed. A reconstituted nanoparticle, synthetic high-density lipoprotein (sHDL), which mimics the native HDL, has been established as clinically safe and is easily manufactured on a large scale. In this study, we propose that the delivery of the antiplatelet drug ML355, a selective inhibitor of 12(S)-lipoxygenase (12-LOX), by sHDL will efficiently inhibit thrombosis by targeting ML355 to the intended site of action, improving the pharmaceutical profile and harnessing the innate antithrombotic efficacy of the sHDL carrier. Our data show that ML355-sHDL exhibits more potent inhibition of thrombus formation in both small arterioles and larger arteries in mice without impairing the normal hemostasis in vivo.Remyelination failure in multiple sclerosis (MS) is associated with a migration/differentiation block of oligodendroglia. The reason for this block is highly debated. It could result from disease-related extrinsic or intrinsic regulators in oligodendroglial biology. To avoid confounding immune-mediated extrinsic effect, we used an immune-deficient mouse model to compare induced pluripotent stem cell-derived oligodendroglia from MS and healthy donors following engraftment in the developing CNS. We show that the MS-progeny behaves and differentiates into oligodendrocytes to the same extent as controls. They generate equal amounts of myelin, with bona fide nodes of Ranvier, and promote equal restoration of their host slow conduction. MS-progeny expressed oligodendrocyte- and astrocyte-specific connexins and established functional connections with donor and host glia. Thus, MS oligodendroglia, regardless of major immune manipulators, are intrinsically capable of myelination and making functional axo-glia/glia-glia connections, reinforcing the view that the MS oligodendrocyte differentiation block is not from major intrinsic oligodendroglial deficits.V2a neurons are a genetically defined cell class that forms a major excitatory descending pathway from the brainstem reticular formation to the spinal cord. Their activation has been linked to the termination of locomotor activity based on broad optogenetic manipulations. However, because of the difficulties involved in accessing brainstem structures for in vivo cell type-specific recordings, V2a neuron function has never been directly observed during natural behaviors. Here, we imaged the activity of V2a neurons using micro-endoscopy in freely moving mice. We find that as many as half of the V2a neurons are excited at locomotion arrest and with low reliability. Other V2a neurons are inhibited at locomotor arrests and/or activated during other behaviors such as locomotion initiation or stationary grooming. Our results establish that V2a neurons not only drive stops as suggested by bulk optogenetics but also are stratified into subpopulations that likely contribute to diverse motor patterns.